Ji Lupeng, Huang Yucun, Zhang Yi, Peng Anping, Qin Jilong, Lu Shaofan, Huang Yu
Department of Medicine, The Fifth People's Hospital of Zhuhai, Zhuhai 519055, People's Republic of China.
Department of Radiology, The Fifth People's Hospital of Zhuhai, Zhuhai 519055, People's Republic of China.
Onco Targets Ther. 2020 Oct 22;13:10729-10738. doi: 10.2147/OTT.S260436. eCollection 2020.
Non-small-cell lung cancer (NSCLC) is the leading cause of cancer-related mortality worldwide. However, the molecular mechanism of NSCLC remains unknown. Accumulating data show that Rhotekin 2 (RTKN2) functions as a novel crucial regulator of diverse biological processes; however, its pathological role in NSCLC remains unclear.
In this study, we investigated the function of RTKN2 in NSCLC. The expression of RTKN2 mRNA was analyzed in tumor tissues and paired adjacent tissues from patients by qRT-PCR. The role of RTKN2 in cell proliferation, apoptosis, migration, and invasion was investigated. The potential mechanisms were explored.
We found that the level of RTKN2 mRNA was up-regulated in NSCLC tissues and cell lines. RTKN2 knockout inhibited the proliferation of human NSCLC cell lines A549 via inducing apoptosis by increasing the level of Bax and decreasing the level of Bcl-2. Furthermore, silencing of RTKN2 reduced the migration and invasion of A549 cells through up-regulated matrix metalloproteinase-9 (MMP9) and MMP2 expression.
These data suggest that RTKN2 may not only be a prognostic biomarker candidate but also provide a potential therapeutic target for NSCLC diagnosis and treatment.
非小细胞肺癌（NSCLC）是全球癌症相关死亡的主要原因。然而，NSCLC的分子机制仍不清楚。越来越多的数据表明，Rhotekin 2（RTKN2）作为多种生物学过程的新型关键调节因子发挥作用；然而，其在NSCLC中的病理作用仍不清楚。
在本研究中，我们研究了RTKN2在NSCLC中的功能。通过qRT-PCR分析患者肿瘤组织和配对的相邻组织中RTKN2 mRNA的表达。研究了RTKN2在细胞增殖、凋亡、迁移和侵袭中的作用。探索了潜在机制。
我们发现NSCLC组织和细胞系中RTKN2 mRNA水平上调。RTKN2基因敲除通过增加Bax水平和降低Bcl-2水平诱导凋亡，从而抑制人NSCLC细胞系A549的增殖。此外，RTKN2沉默通过上调基质金属蛋白酶-9（MMP9）和MMP2表达降低A549细胞的迁移和侵袭。
这些数据表明，RTKN2不仅可能是一种预后生物标志物候选物，而且为NSCLC的诊断和治疗提供了潜在的治疗靶点。
